SEVEN-LAYER FRAMEWORK × SIX MODULES
七層框架 × 六系統
每一層只記一件事：是什麼 → 怎麼走 → 綁什麼 → 然後呢 → 哪裡相反 → 藥物怎麼介入 → 阻斷的代價。
你要存的是層的順序，內容留在後端。換系統時順序完全不變。中英對照，考試用英文寫。
01為什麼是七層
任何藥理學題目，無論哪一堂課，都是這七層的展開。
| 層 | 問什麼 | 這是全課唯一需要記死的順序 |
|---|
| 1 | 這是什麼系統？ | 系統的性質與目的 |
| 2 | 訊息或藥物怎麼走？ | 路徑與順序 |
| 3 | 綁什麼？用哪個 port？ | 配體、受體、亞型 |
| 4 | 綁定之後怎麼執行？ | 第二傳訊者與訊號鏈 |
| 5 | 哪裡方向相反？ | 最容易記錯的那一點 |
| 6 | 藥物怎麼介入？ | 機制軸（直接／間接） |
| 7 | 阻斷的代價？ | 副作用從哪來 |
The seven layers are the same for every module. Only layer 3 and layer 4 change names. 這就是換系統不用重讀的原因。
02L1 PK｜藥動學
層 1
系統
這是什麼系統
PK 回答的是「身體對藥物做了什麼」，與 PD（藥物對身體做了什麼）相反。藥物從進入到離開身體會經過四個階段：吸收、分佈、代謝、排泄。
Pharmacokinetics describes what the body does to the drug, and passes through four stages: absorption, distribution, metabolism, excretion.
層 2
路徑
訊息怎麼走
口服藥物走完整條路：腸道吸收 → 門靜脈 → 肝臟 → 全身循環 → 腎臟或膽汁。靜脈注射跳過前段，所以是 100% 基準。口服藥會先經過腸壁與肝臟的首次通過代謝，因此損失生物利用度。
An oral drug travels gut to portal vein to liver to circulation to kidney or bile. Intravenous dosing skips the early steps, which is why it is the 100% baseline, while oral drugs lose bioavailability to first-pass metabolism in the gut wall and liver.
層 3
綁定
綁什麼
藥物被血漿蛋白結合限制。結合態分子體積大、無法通過毛細血管壁，所以只有游離型才有活性、能通過血腦屏障、並被腎小球濾過。
Protein binding limits the drug. The bound form is large in volume and cannot cross capillary walls, so only the free fraction is active, crosses the blood-brain barrier, and is filtered by the glomerulus.
層 4
執行
綁定之後怎麼執行
代謝分兩階段。Phase I 由 CYP450 主導，多數不改變活性，但藥物之間的交互作用主要發生在這裡，因為酵素的誘導或抑制會改變藥物濃度。Phase II 做結合反應，把產物變成水溶性以便排泄。
Metabolism has two phases. Phase I is driven by CYP450 and usually preserves activity, but it is where most drug interactions occur because enzyme induction or inhibition changes drug levels. Phase II conjugates the product so it becomes water-soluble for excretion.
層 5
相反
哪裡方向相反
弱酸與弱鹼的處理方向完全相反。弱酸性藥物在酸性尿液中未解離、脂溶性高，所以被再吸收回血液，因此鹼化尿液可加速排出。弱鹼性藥物則相反，需要酸化尿液。
Weak acids and weak bases are handled in opposite directions. A weak acid is unionised in acidic urine and lipid-soluble, so it is reabsorbed, which means alkalinising the urine speeds its removal. Weak bases need the opposite treatment.
層 6
介入
藥物怎麼介入
給藥途徑的選擇就是介入方式。舌下給藥繞過首渡，因為首渡代謝會在藥物到達循環前就把它破壞。藥物設計也可以介入，例如去兒茶酚環的改造讓藥物逃過酵素降解。
Route of administration is the intervention. Sublingual dosing bypasses first-pass metabolism, which would otherwise destroy the drug before it reached circulation. Structural design also intervenes, as removing the catechol ring lets a drug escape enzymatic degradation.
層 7
代價
阻斷的代價
分子量決定了唯一的出口。約 300 Da 以下的藥物走尿液，超過 500 Da 走膽汁，因此中間分子量的藥物需要代謝轉換才能排泄。與 Probenecid 併用會抑制主動分泌，讓 Penicillin 濃度升高。
Molecular weight decides the only available exit. Drugs under about 300 daltons leave through urine and those over 500 through bile, so mid-range drugs must be metabolised first. Co-administration with probenecid also inhibits active secretion and raises penicillin levels.
03L2 PD｜藥效學
層 1
系統
這是什麼系統
藥效學是藥物與受體結合後產生效應的系統，核心是一個可逆的化學平衡。因為平衡可逆，所以提高濃度可以把受體全部佔據，阻斷劑也只能把效應推回來。
Pharmacodynamics converts drug-receptor binding into effect, built on a reversible equilibrium. Because it is reversible, raising concentration can occupy every receptor, and an antagonist can only push the effect back.
層 2
路徑
訊息怎麼走
基本式是游離藥物濃度加上游離受體，結合成複合體後產生效應。游離濃度而非總濃度才是有效濃度，所以藥物結合蛋白後實際能作用的量會下降。
The core equation is free drug plus free receptor forming a complex that produces effect. Free rather than total concentration is what matters, so protein binding reduces the amount actually available.
層 3
綁定
綁什麼
受體分四大類。離子通道型（菸鹼型 N）最直接；GPCR 分三種耦合；核受體在細胞內、作用慢但持久；受體酪胺酸激酶如胰島素。
Receptors fall into four families. Ion channels such as the nicotinic receptor are the most direct; GPCRs come in three couplings; nuclear receptors sit inside the cell and act slowly but durably; receptor tyrosine kinases such as insulin complete the list.
層 4
執行
綁定之後怎麼執行
G 蛋白的亞型決定了第二傳訊者，而第二傳訊者決定方向。Gq 走 IP₃ 與 DAG 並升高鈣離子；Gi 降低 cAMP；Gs 升高 cAMP。口訣是 QISS。
The G-protein subtype determines the second messenger, and the second messenger determines direction. Gq raises calcium through IP₃ and DAG, Gi lowers cAMP, and Gs raises cAMP.
層 5
相反
哪裡方向相反
Kd 不等於 ED50，因為一個描述結合、一個描述效應，而效應還受備用受體與訊號放大影響。效價與效能也互相獨立，所以效價高不代表效能高。
Kd does not equal ED₅₀ because one describes binding and the other describes effect, and the effect also depends on receptor reserve and signal amplification. Potency and efficacy are likewise independent.
層 6
介入
藥物怎麼介入
激動劑與拮抗劑的差別在於是否產生內生活性。全致效劑為 1，部分致效劑小於 1。拮抗劑分競爭性與非競爭性：競爭性結合同一位點、非競爭性結合異位點或堵住通道。
Agonists and antagonists differ in intrinsic activity. A full agonist has an intrinsic activity of 1 and a partial agonist has less. Antagonists are competitive or non-competitive: competitive binds the same site, non-competitive binds elsewhere or blocks the channel.
層 7
代價
阻斷的代價
長期使用致效劑會讓受體下降調節，而下降有兩種方式。去敏感化是磷酸化使受體與 G 蛋白脫鉤，快速可逆且受體數量不變；下調是受體被內吞降解，緩慢且受體數量真的減少。
Chronic agonist use causes downregulation, and there are two forms. Desensitisation is phosphorylation that uncouples the receptor from the G protein, fast and reversible with receptor numbers unchanged. Downregulation is internalisation and degradation, slow, with receptor numbers actually falling.
04L3 ANS｜自主神經系統本週三道大題都在考這科
層 1
系統
這是什麼系統
這是一個雙節點的訊息系統，交感與副交感控制同一批效應器但方向相反。交感負責應付緊急，副交感負責恢復與儲存，腸神經系統則可獨立運作。
This is a two-node signalling system in which sympathetic and parasympathetic control the same effectors in opposite directions. Sympathetic handles emergencies, parasympathetic restores and stores, and the enteric system can run independently.
層 2
路徑
訊息怎麼走
訊號走三段：節前纖維、神經節、節後纖維再到效應器。關鍵在於節前纖維的傳遞物質固定不變，因為交感與副交感在神經節處無法區分，所以必定使用同一種物質，而節後才分化出系統身份。
The signal passes through three stages: pre-ganglionic fibre, ganglion, post-ganglionic fibre, then effector. Pre-ganglionic transmission is fixed because the two divisions cannot be distinguished at the ganglion, so the same transmitter is used and identity only emerges after the ganglion.
層 3
綁定
綁什麼 — Q1 的核心
所有節前纖維都是 ACh 作用在菸鹼型受體。節後副交感仍是 ACh 但改用毒蕈鹼型受體，節後交感改用正腎上腺素作用在腎上腺素受體。唯一例外是汗腺，交感節後纖維釋放 ACh 而非 NE。
藥物分四象限：擬交感（Epi、Salbutamol）、抗交感（Metoprolol、Phentolamine）、擬副交感（Bethanechol、Neostigmine）、抗副交感（Atropine、Ipratropium）。
All pre-ganglionic fibres use acetylcholine on nicotinic receptors. Post-ganglionic parasympathetic fibres keep acetylcholine but switch to muscarinic receptors, while post-ganglionic sympathetic fibres switch to norepinephrine on adrenoceptors. The single exception is the sweat gland, where sympathetic fibres release acetylcholine.
層 4
執行
綁定之後怎麼執行 — Q2 的核心
腎上腺素受體的亞型決定一切。α1 走 Gq 升高鈣離子使血管收縮，α2 走 Gi 抑制正腎上腺素釋放，β1 走 Gs 使心跳加快，β2 走 Gs 使平滑肌舒張，β3 走 Gs 使膀胱舒張。毒蕈鹼型中奇數是 Gq、偶數是 Gi，菸鹼型是離子通道所以最快。
The adrenoceptor subtype determines everything. α1 uses Gq to raise calcium and constrict vessels, α2 uses Gi to inhibit norepinephrine release, β1 uses Gs to speed the heart, β2 uses Gs to relax smooth muscle, and β3 uses Gs to relax the bladder. Among muscarinic receptors the odd numbers are Gq and the even numbers are Gi, while nicotinic receptors are ion channels and therefore fastest.
層 5
相反
哪裡方向相反 — 最容易記錯
同一條 Gs 鏈在不同效應器上方向相反，在心肌造成收縮、在平滑肌造成舒張。原因是心肌靠鈣離子收縮，平滑肌靠 cAMP 激活 MLCP 移除磷酸基而無法結合。所以平滑肌裡 Gq 收縮、Gs 舒張。
The same Gs chain runs in opposite directions in different effectors, contracting cardiac muscle but relaxing smooth muscle. Cardiac muscle contracts because calcium rises, while smooth muscle relaxes because cAMP activates MLCP and removes the phosphate groups needed for binding.
層 6
介入
藥物怎麼介入 — Q3 的核心
三種介入方式。直接型自己結合受體；間接型提高體內既有的正腎上腺素，三種手法分別是搬出囊泡儲存、阻斷回收、阻斷代謝；混合型兩者兼具。結構上，去掉兒茶酚環的非兒茶酚胺能逃過 COMT 與 MAO，因此可口服且半衰期長。
There are three modes of intervention. Direct agents bind the receptor themselves. Indirect agents raise existing norepinephrine by mobilising vesicular stores, blocking reuptake, or blocking metabolism. Mixed agents do both. Structurally, non-catecholamines lack the catechol ring, escape COMT and MAO, and so become orally viable with a longer half-life.
層 7
代價
阻斷的代價
阻斷的代價來自被關掉的受體原本負責什麼。阻斷 β2 使支氣管無法舒張而痙攣，所以非選擇性 β 阻斷劑在氣喘禁忌。阻斷 α2 移除突觸前負反饋，反而使正腎上腺素釋放增加而血壓反升。
The cost of blockade equals what the blocked receptor normally does. Blocking β2 prevents bronchial relaxation and causes spasm, so non-selective beta blockers are contraindicated in asthma. Blocking α2 removes presynaptic negative feedback, so norepinephrine release increases and blood pressure rises instead of falling.
05L4 CVS｜心血管範圍最大 · 分數密度最高
層 1
系統
這是什麼系統
心血管系統是幫浦加上管路加上調節。血壓等於心輸出乘以全身血管阻力，所以要降血壓只有三條路：降低心輸出、降低血管阻力、或兩者同時做。
The cardiovascular system is a pump, a set of pipes and a regulator. Blood pressure equals cardiac output times systemic vascular resistance, so there are only three ways to lower it: reduce output, reduce resistance, or both.
層 2
路徑
訊息怎麼走
調節訊號來自三套系統：交感神經、腎素血管張力素醛固酮系統、以及壓力感受器反射。前兩套升高血壓，第三套在血壓過高時反射性減慢心跳，所以高血壓常伴隨心跳減慢。
Three systems deliver regulatory signals: the sympathetic nervous system, the renin-angiotensin-aldosterone system, and the baroreceptor reflex. The first two raise blood pressure while the third reflexively slows the heart when pressure is high, so hypertension often comes with bradycardia.
層 3
綁定
綁什麼 — ABCD 四個作用點
降血壓藥物有四個作用點。腎上腺素受體作用在血管與心臟，鈣離子通道阻斷劑分血管選擇與心臟選擇兩類，腎素血管張力素系統靠 ACE 與 Ang II 受體，利尿劑作用在腎臟的再吸收位置。
診斷需非同日三次血壓均偏高；分期有三套標準，答題必須寫明引用哪一套。
Antihypertensives act at four points. Adrenoceptors act on vessels and heart, calcium channel blockers split into vessel-selective and heart-selective, the renin-angiotensin system is targeted through ACE and the angiotensin receptor, and diuretics act on renal reabsorption sites.
層 4
執行
綁定之後怎麼執行
四個槓桿各有用不同的訊號機制。ACEI 阻斷 Ang I 轉成 Ang II 並減少醛固酮。β1 阻斷劑降低心率與腎素。Dihydropyridine 類阻斷血管的鈣內流。利尿劑阻斷鈉的再吸收而讓鈉從尿中排出。
Each lever uses a different mechanism. ACE inhibitors block the conversion of angiotensin I and reduce aldosterone. Beta-1 blockers lower heart rate and renin. Dihydropyridine calcium channel blockers block calcium entry into vessels. Diuretics block sodium reabsorption so sodium leaves through urine.
層 5
相反
哪裡方向相反 — 兩組
第一組：環利尿劑低血鈣、Thiazide 高血鈣，因為環利尿劑阻斷鈉的同時也阻斷鈣的被動再吸收，而 Thiazide 作用處的鈣仍可主動運輸。
第二組：非 Dihydropyridine 類鈣離子通道阻斷劑作用在心臟而非血管。
Loop diuretics block sodium and with it the passive reabsorption of calcium, causing hypocalcaemia, whereas thiazides leave calcium transport intact and cause hypercalcaemia. Non-dihydropyridine calcium channel blockers act on the heart rather than vessels.
層 6
介入
藥物怎麼介入 — Vaughan Williams 四類
抗心律不整藥物依機轉分為四類，依序阻鈉通道、阻斷 β 受體、阻鉀通道、阻鈣通道。口訣是一鈉、二貝、三鉀、四鈣。第一類具有使用依賴性，因為它結合鈉通道的不活化狀態，心率越快、不活化通道比例越高，阻斷就越強。
Antiarrhythmics are grouped by mechanism into four classes blocking sodium channels, beta receptors, potassium channels and calcium channels in turn. Class one shows use-dependence because it binds the inactivated state of the sodium channel, so a faster rate means more inactivated channels and stronger blockade.
層 7
代價
阻斷的代價
阻斷的代價包括乾咳與高血鉀。ACE 也分解 Bradykinin，所以抑制 ACE 會讓 Bradykinin 累積而刺激呼吸道產生乾咳；Ang II 下降使醛固酮減少，腎臟排鉀減少而高血鉀。雙側腎動脈狹窄時禁用 ACEI，因為腎灌流壓正靠 Ang II 維持。
Digoxin 改善症狀與住院率但不改善生存；β 阻斷劑改善生存，但需低劑量起始、約三個月才完整生效。
The costs of blockade include cough and hyperkalaemia. ACE also degrades bradykinin, so inhibiting it lets bradykinin accumulate and stimulate the airway, causing dry cough. Falling angiotensin II reduces aldosterone, so the kidney excretes less potassium and potassium rises. ACE inhibitors are contraindicated in bilateral renal artery stenosis because glomerular filtration pressure depends on angiotensin II.
06L5 Resp｜呼吸
層 1
系統
這是什麼系統
呼吸系統有兩件互相獨立的事：氣道張力與氣道發炎。支氣管擴張只處理前者，抗發炎藥處理後者，兩者缺一不可。
The respiratory system has two independent problems: airway tone and airway inflammation. Bronchodilation handles only the first and anti-inflammatory drugs handle the second, so neither alone is sufficient.
層 2
路徑
訊息怎麼走
支氣管平滑肌同時受交感與副交感支配。交感經 β2 使平滑肌舒張，副交感經 M3 使平滑肌收縮，所以哮喘是這條平衡被打破的結果。
Bronchial smooth muscle is under both sympathetic and parasympathetic control. Sympathetic β2 relaxes it while parasympathetic M3 contracts it, so asthma is a breakdown of that balance.
層 3
綁定
綁什麼
三類支氣管擴張劑綁三個不同目標：β2 致效劑 bind β2 受體，抗膽鹼藥阻斷 M3，Theophylline 抑制磷酸二酯酶以維持 cAMP。
四類抗發炎藥分別作用在發炎介質的生成、受體、合成酵素、細胞脫顆粒與分解酵素。
Three bronchodilator classes target three different things: beta-2 agonists bind β2 receptors, antimuscarinics block M3, and theophylline inhibits phosphodiesterase to maintain cAMP. Four anti-inflammatory classes act on mediator generation, the receptor, the synthesis enzyme, cell degranulation, and the breakdown enzyme.
層 4
執行
綁定之後怎麼執行
β2 走 Gs 升高 cAMP，cAMP 激活 MLCP讓肌球蛋白輕鏈去磷酸化而無法與肌動蛋白結合，因此平滑肌舒張。支氣管擴張就是這條鏈的結果。
β2 uses Gs to raise cAMP, and cAMP activates MLCP so the myosin light chain loses its phosphate groups and cannot bind actin, which relaxes smooth muscle. Bronchodilation is the result of this chain.
層 5
相反
哪裡方向相反
緩解藥與控制藥的時間方向相反。控制藥（吸入類固醇）作用在生成端，需要誘導新蛋白質合成，所以要數小時至數天；緩解藥（SABA）直接作用在效應端的肌肉上，所以是分鐘級。急性發作時控制藥來不及。
另一處：哮喘是發炎為主所以必須用類固醇，慢性阻塞性肺病是擴張為主所以用 LAMA 與 LABA，類固醇效果較差。
Controllers such as inhaled steroids act on the generation side and require new protein synthesis, taking hours to days, while relievers such as short-acting beta-2 agonists act directly on the effector muscle within minutes. During an acute attack the controller arrives too late.
層 6
介入
藥物怎麼介入 — 兩條階梯
兩條治療階梯方向相反。哮喘階梯往上是加抗發炎藥，核心是吸入類固醇；慢性阻塞性肺病階梯往上是加支氣管擴張藥，核心是 LAMA 與 LABA。
LABA 不能單獨用於哮喘，因為它只舒張支氣管卻不控制發炎，會掩蓋症狀而讓發炎繼續累積。
The two treatment ladders run in opposite directions. The asthma ladder adds anti-inflammatory therapy upward with inhaled steroids at its core, while the COPD ladder adds bronchodilation upward with LAMA and LABA at its core.
層 7
代價
阻斷的代價
第一代抗組織胺阻斷 M 受體但脂溶性高能通過血腦屏障，所以產生嗜睡——而嗜睡正好可用來治暈車。去充血劑阻斷 α1 讓鼻黏膜血管收縮而消肿，但長期使用使受體下調，產生反彈性充血。Theophylline 治療窗窄，需監測血中濃度。
The cost of blockade shows in the side effects. First-generation antihistamines block muscarinic receptors but are lipid-soluble enough to cross the blood-brain barrier, so they sedate. Decongestants block α1 to shrink nasal vessels, but long-term use downregulates receptors and causes rebound congestion.
07L6 CNS｜中樞神經
層 1
系統
這是什麼系統
中樞神經系統是一個受血腦屏障保護的控制中心，所以藥物能不能進去是第一步問題。進去之後才談得上作用機制。
The central nervous system is a control centre protected by the blood-brain barrier, so whether a drug can enter is the first question. Only after entry does mechanism matter.
層 2
路徑
訊息怎麼走
訊號沿著神經元傳遞，最後由神經傳遞物質作用於受體。多數神經傳遞物質是胺類或胜肽，其中許多藥物正是模仿或阻斷這些傳遞物質。
Signals travel along neurons and finally act through neurotransmitters on receptors. Most neurotransmitters are amines or peptides, and many drugs either mimic or block them.
層 3
綁定
綁什麼
要能進入血腦屏障，藥物必須是小分子量、脂溶性高、且非解離狀態。通過之後才作用於特定受體，例如阿片類的 μ 受體、抗癲癇藥的 GABA 或 AMPA 受體、止吐藥的 5-HT₃ 或 NK₁ 受體。
三重代價：脂溶性越高 → 進得去、中樞活性越高、脂肪滯留越多、停藥後效應越久。
To cross the blood-brain barrier a drug must be small, lipid-soluble and unionised. Only after entry does it act on a specific receptor, such as the mu receptor for opioids, GABA or AMPA receptors for antiepileptics, and serotonin or NK1 receptors for antiemetics.
層 4
執行
綁定之後怎麼執行 — 抗癲癇兩隊
抗癲癇藥有兩種相反策略。強化 GABA 的藥物增加抑制作用，例如苯巴比妥延長氯離子通道開啟時間、苯二氮平增加開啟頻率、Gabapentin 結合鈣通道次單元；另一種直接掐斷興奮性傳遞，例如 Perampanel 阻斷 AMPA 受體、Ezogabine 開啟鉀通道使細胞超極化。兩者目標都是讓神經元難以達到閾值。
Antiepileptics use two opposite strategies. Those enhancing GABA increase inhibition, with barbiturates lengthening chloride channel opening and benzodiazepines increasing its frequency. The other group cuts off excitatory transmission, with perampanel blocking AMPA receptors and ezogabine opening potassium channels to hyperpolarise the cell. Both aim to make the neuron harder to bring to threshold.
層 5
相反
哪裡方向相反
COX-1 與 COX-2 的功能相反。COX-1 處理日常維持工作，例如保護胃黏膜與產生血小板因子；COX-2 只在發炎組織被誘導，腫痛熱就是它造成的。COX-2 選擇性抑制劑胃腸道副作用較少但心血管風險較高。
Aspirin 不可逆乙醯化 COX，所以同時有抗血小板作用與胃腸道副作用。
COX-1 handles daily housekeeping such as gastric protection and platelet production, while COX-2 is induced only at inflamed tissue and produces swelling, pain and heat. Selective COX-2 inhibitors cause fewer gastrointestinal problems but carry higher cardiovascular risk.
層 6
介入
藥物怎麼介入
藥物分直接與間接。直接作用於受體，例如阿片類；間接提高體內既有的傳遞物質，例如抑制乙醯膽鹼酯酶讓乙醯膽鹼堆積。
止吐藥的選擇由觸發來源決定而非嚴重程度：5-HT₃ 處理化療與術後、NK₁ 處理急性與延遲性、M 受體處理動暈。
Drugs act either directly on receptors, as opioids do, or indirectly by raising existing transmitters, as acetylcholinesterase inhibitors do by letting acetylcholine accumulate. Antiemetics are chosen by trigger rather than severity.
層 7
代價
阻斷的代價 — 兩個反直覺
阿片類阻斷 μ 受體會同時抑制呼吸中樞而導致呼吸抑制，這是致死主因。長期使用苯二氮平使 GABA 受體下調，產生耐受性與依賴性，所以長期抗焦慮首選 SSRI 而不是苯二氮平。
膽鹼酯酶抑制劑只改善症狀，因為阿茲海默的病因是神經元退化，抑制酵素並不阻止神經元死亡。
Blocking mu receptors with an opioid also suppresses the respiratory centre, which is the main cause of death. Chronic benzodiazepine use downregulates GABA receptors, producing tolerance and dependence, which is why long-term anxiety treatment uses SSRIs instead. Cholinesterase inhibitors improve symptoms only, because Alzheimer's is caused by neuronal degeneration.
08跨系統對照換系統不用重讀的真正用法
同一個底層陷阱，在六科換了不同外觀。看到左欄應該能填出右欄。
| 底層陷阱 | L3 ANS | L4 CVS | L5 Resp | L6 CNS | L1 PK |
|---|
同一機制
方向相反 | Gs 在心肌收縮、平滑肌舒張 | 環利尿劑低血鈣、Thiazide 高血鈣 | 緩解藥分鐘級、控制藥天級 | COX-1 維持、COX-2 發炎 | 弱酸鹼化、弱鹼酸化 |
阻斷
產生代償 | 阻斷 α2 使 NE↑ | 阻斷 α1 使 GFR↓ | 去充血劑長期致反彈性充血 | 阻斷 μ 致呼吸抑制 | 結合率高則游離低 |
分佈決定
副作用 | β2 在肺、β1 在心 | α1 在血管、β1 在腎 | M3 在腺體與平滑肌 | μ 在呼吸中樞 | 結合態不能過膜 |
酵素決定
能不能口服 | 非兒茶酚胺可口服 | — | LABA 不能單獨用 | 一代抗組織胺過 BBB | 首渡代謝破壞藥物 |
| 量與競爭 | 阻斷 β2 需加量競爭 | 使用依賴性 | LABA 掩蓋發炎 | 部分致效劑變拮抗劑 | 抑制分泌可被競爭 |
09筆答格式
每一層寫 1–3 句完整句子，不要用 bullet point。以下示範 L3 層 3。
All pre-ganglionic fibres use acetylcholine on nicotinic receptors, because sympathetic and parasympathetic fibres cannot be distinguished at the ganglion. Post-ganglionic parasympathetic fibres continue to use acetylcholine but switch to muscarinic receptors, whereas post-ganglionic sympathetic fibres switch to norepinephrine on adrenoceptors. The single exception is the sweat gland, where sympathetic post-ganglionic fibres release acetylcholine rather than norepinephrine.
所有節前纖維都使用乙醯膽鹼作用在菸鹼型受體，因為交感與副交感在神經節處無法區分。節後副交感纖維仍使用乙醯膽鹼但改為毒蕈鹼型受體，節後交感纖維則改用正腎上腺素作用在腎上腺素受體。唯一例外是汗腺，其交感節後纖維釋放的是乙醯膽鹼而非正腎上腺素。
寫作原則
- 每段開頭用連接詞點出邏輯關係——because、therefore、however、while
- 有例外就一定要寫，因為例外是拿分點
- 藥名先寫機制，機制先寫推導，這樣即使忘了藥名也有分
- 不要為了長度而寫超出題目範圍的內容，教授說過不要炫技
10數字與分期待查
數字
90%
Nitroglycerin 首渡代謝 → 舌下給藥
25% / 5%
環利尿劑 / Thiazide 阻斷比例
100×
Fentanyl 對 Morphine 效價倍數
血壓分期（三套並列，答題必須寫明出處）
| 分類 | ACC/AHA 2017 | JNC7 | 香港衞生署 CHP |
|---|
| 正常 | <120 / <80 | <120 / <80 | <120 / <80 |
| 升高或前期 | 120–129 / <80 | 120–139 / 80–89 | 120–139 / 80–89 |
| 一期 | 130–139 / 80–89 | 140–159 / 90–99 | 不以此分類 |
| 二期 | ≥140 / ≥90 | ≥160 / ≥100 | — |
| 診斷門檻 | ≥130 / ≥80 | ≥140 / ≥90 | ≥140 / ≥90 |
安全答法：Always state which guideline you cite. Writing all three with their sources means the marker cannot deduct for ambiguity.
考場四層篩選（拿到 6 題之後）
- 30 秒，只分類不動筆 — 哪幾題屬於我強的模組
- 每題 20 秒 — 能列出 6 個具體點嗎？不能就淘汰
- 30 秒 — 能照七層寫滿一頁嗎？不能就降級
- 挑最高的 4 題，落選的兩題一秒都不要再讀
保險底線是 4 門。只強 3 門的話，命運決定 6 題中有 4 題來自不熟的模組就會崩。寧可 4 題寫滿、2 題完全空白，也不要 6 題都半殘。